Recombination-dependent mutation in Escherichia coli occurs in stationary phase

• Published in: Genetics (Austin) 1998-06, Vol.149 (2), p.1163-1165
• Main Authors: McKenzie, G J, Lombardo, M J, Rosenberg, S M
• Format: Article
• Language: English
• Subjects: Escherichia coli - genetics; Escherichia coli - growth & development; Interphase - genetics; Letter; Mutation; Recombination, Genetic
• ISSN: 0016-6731; 1943-2631; 1943-2631
• DOI: 10.1093/genetics/149.2.1163

"Adaptive" or "stationary-phase" mutation occurs in apparently stationary-phase population of cells, over time, after exposure to a nonlethal selection. In one assay system, Escherichia coli with an amber mutation in lacZ forms Lac super(+) colonies over time when plated on medium with lactose as the sole carbon source (Cairns et al. 1988). These Lac super(+) mutations had been postulated to form after exposure to, and in response to, the selective medium (Cairns et al. 1988), but in an article in Genetics last year, most of these were shown to be slow-growing mutants that formed during preselective growth of the culture (Prival and Cebula 1996). For the lac amber reversion assay system, the hypothesis of mutations occurring by a different mechanism after plating is not supported. Is this generally the case? In a well-characterized system for studying presumed stationary-phase mutation, E. coli with a lacI-lacZ fusion gene with a +1 frameshift mutation appears to revert to Lac super(+) over time after exposure to minimal medium with lactose as the sole carbon source (Cairns and Foster 1991). In this system, the late arising Lac super(+) mutants form via a different molecular mechanism from the early mutants (reviewed by Bridges 1997; Rosenberg 1994, 1997; Rosenberg et al 1995; 1996, 1998). The late appearing mutations (1) require proteins of the RecBCD recombination system to form (Harris et al. 1994, 1996; Foster et al. 1996); (2) possess a unique mutation spectrum mostly of -1 deletions at mononucleotide repeats (Foster and Trimarchi 1994; Rosenberg et al. 1994); (3) arise in a hypermutable subpopulation of cells whose whole genome is susceptible to mutation (Torkelson et al. 1997); and (4) occur in cells in which postsynthesis mismatch repair activity is diminished transiently at the level of limiting MutL protein (Longerich et al. 1995; Harris et al. 1997; Rosenberg et al. 1998). Early arising mutants have different sequences, are rec and ruv gene-independent, and form under conditions in which mismatch repair protein MutL is not limiting.